development of the social brain during adolescence

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Development of the social brain duringadolescenceSarah-Jayne Blakemore aa Institute of Cognitive Neuroscience, University College London , London,UKPublished online: 30 Sep 2010.

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Development of the social brain during adolescence

Sarah-Jayne BlakemoreInstitute of Cognitive Neuroscience, University College London, London, UK

Adolescence is usually defined as the period of psychological and social transition between childhoodand adulthood. The beginning of adolescence, around the onset of puberty, is characterized by largehormonal and physical changes. The transition from childhood to adulthood is also characterized bypsychological changes in terms of identity, self-consciousness, and cognitive flexibility. In the pastdecade, it has been demonstrated that various regions of the human brain undergo developmentduring adolescence and beyond. Some of the brain regions that undergo particularly protracted devel-opment are involved in social cognitive function in adults. In the first section of this paper, I brieflydescribe evidence for a circumscribed network of brain regions involved in understanding otherpeople. Next, I describe evidence that some of these brain regions undergo structural developmentduring adolescence. Finally, I discuss recent studies that have investigated social cognitive develop-ment during adolescence.

The first time Uta Frith made an impression onme was when I was 15. That year I was given acopy of her book Autism: Explaining the Enigma(U. Frith, 1989), which had recently been pub-lished. I knew nothing about autism and foundUta’s book captivating. It inspired me to write toits author and ask if I could do a week’s workexperience in her lab. With characteristic generos-ity, Uta agreed. So in the summer of 1990, I spenta week in the Medical Research Council (MRC)Cognitive Development Unit, where I observedchildren with autism being tested on the SallyAnne task, and joined in when Uta’s group weregenerating spoonerisms like Dob Bylan andHimi Jendrix. At the time, I didn’t quite realisethat this research had revolutionized what isknown about autism and dyslexia. Together withSimon Baron-Cohen and Alan Leslie, Uta had

just a few years earlier published the first paperto show that children with autism have problemspassing Theory of Mind tasks. If you search for[Theory of Mind in autism] on the web todayyou get over one million entries! Uta’s work onautism and dyslexia is not just renownedamongst scientists, but has also made a significantimpact on teachers, clinicians, carers, and parents.Doing work experience with Uta all those yearsago was truly inspirational.

I met Uta again when I was doing a PhD withChris Frith. In 2000, Uta asked me to help herwrite a report for the Economic and SocialResearch Council (ESRC) on the implications ofbrain research for education. Uta had the visionto realise that this would soon become an import-ant area of science. Indeed, brain and educationresearch is now a flourishing discipline in itself,

Correspondence should be addressed to Sarah-Jayne Blakemore, Institute of Cognitive Neuroscience, University College

London, 17 Queen Square, London WC1N 3AR, UK. E-mail: [email protected]

I am grateful to the Royal Society, UK, which funds my research.

40 # 2008 The Experimental Psychology Society

http://www.psypress.com/qjep DOI:10.1080/17470210701508715

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with ring-fenced funding, dedicated internationalconferences, books, and a new journal. Whilewriting the ESRC report, Uta and I were struckby the scarcity of literature on brain research thatwas aimed at educators. This seemed curioussince some areas of brain research are very relevantto education (and in other areas the implicationsare far from clear). In addition, we came acrossthe substantial market of educational tools thatmake claims about the brain. Our experience wasthat there is real interest amongst educatorsabout these claims and the research they arebased on. As a consequence, Uta and I decidedto write a book on the subject (Blakemore &Frith, 2005). On the basis of Uta’s previous well-received and successful books (e.g., U. Frith,1989, 2003; Houston & Frith, 2000), her long-time publisher, Blackwell, agreed to publish ourbook.

One of the areas of brain research that was juststarting to take off at the time we wrote our bookwas development during adolescence. Much isknown (mostly from animal research) aboutbrain changes in the early years. In comparison,at the time of writing our book, there was a largegap in knowledge about brain development afterearly childhood, possibly because the extantresearch was carried out on animal brain tissue,and, unlike humans, animals do not go throughextended periods of adolescent maturity. Therewere a handful of new magnetic resonanceimaging (MRI) studies looking at developmentof the human adolescent brain, and these werepointing to significant waves of change in severalareas of cortex. This was fascinating, not leastbecause several developmental disorders developduring or just after adolescence. For example,schizophrenia is a disorder that usually developsat the end of adolescence. Was it possible thatpostpubescent cortical sculpting does not proceednormally in people who develop schizophrenia?While there are indications that neuropathologyoccurs in early development in schizophrenia(e.g., Weinberger, 1987), recently it has beensuggested that aberrations in neurodevelopmentalprocesses might also take place during the adoles-cent years (McGlashan & Hoffman, 2000). When

Uta and I were researching our book, there wasrelatively little research on brain development intypically developing adolescents and even less onadolescents who later develop schizophrenia.

Another field in which Uta’s research has beeninfluential from the start is social neuroscience.Together with Chris Frith and other colleagues,Uta published some of the first papers in thisnew area. In the next section, I describe evidencefor a network of brain regions dedicated to under-standing others.

The social brain

It is only in the past decade or two that the searchfor the biological basis of social behaviour began(Cacioppo & Berntson, 1992). Uta Frith wasamong the first to study the brain basis of socialcognitive processes, in particular Theory of Mind(ToM; or what Uta termed “mentalizing”).Mentalizing is defined as the ability to attributemental states to other people in order to predicttheir behaviour (e.g., U. Frith & Frith, 2003; seealso Perner & Leekham, 2008 this issue; Sodian,2008 this issue).

Uta and colleagues published one of the firstneuroimaging studies of mentalizing in 1995(Fletcher et al., 1995). In this positron emissiontomography (PET) experiment, subjects readstories that required mental state attribution(ToM stories), stories about physical, naturalevents that did not require any attribution ofmental states (physical stories), and paragraphsmade up of unlinked sentences that were uncon-nected with each other and did not constitute astory. The Theory of Mind (ToM) stories, relativeto unlinked sentences, activated the superior tem-poral sulcus (STS), medial prefrontal cortex(mPFC), precuneus/posterior cingulate cortex,and temporal poles (see Figure 1). Comparedwith the physical stories, the ToM stories activatedthe mPFC and precuneus, as well as the rightinferior parietal cortex adjacent to the temporo-parietal junction (TPJ).

Since this ground-breaking paper, there havebeen dozens of neuroimaging studies investigatingthe neural basis of mentalizing, each showing

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SOCIAL BRAIN DEVELOPMENT

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remarkable agreement with this first study. Here, Ibriefly review the evidence that mentalizing isassociated with activation of the same circum-scribed neural network. Recent neuroimagingstudies, some by Uta Frith’s group, others by labsall over the world, have used a wide range ofstimuli including verbal stories (Gallagher et al.,2000; Saxe & Kanwisher, 2003), sentences (denOuden, Frith, Frith, & Blakemore, 2005; seeFigure 2), words (Mitchell, Heatherton, &Macrae, 2002), cartoons (Brunet, Sarfati, Hardy-Bayle, & Decety, 2000; Gallagher et al., 2000),and animations (Castelli, Happe, Frith, & Frith,2000; see Figure 3). These studies have replicatedthe original finding by Fletcher and colleagues(Fletcher et al., 1995) of activation in mPFC,STS/TPJ, and the temporal poles when subjects

think about mental states (see C. D. Frith &Frith, 2006; U. Frith & Frith, 2003, for review).

The same brain regions have been implicated inmentalizing from lesion studies. In particular,lesions to the frontal cortex (Channon &Crawford, 2000; Gregory et al., 2002; Happe,Malhi, & Checkley, 2001; Rowe, Bullock,Polkey, & Morris, 2001; Stone, Baron-Cohen, &Knight, 1998; Stuss, Gallup, & Alexander, 2001)and STS/TPJ (Apperly, Samson, & Humphreys,2005; Samson, Apperly, Chiavarino, &Humphreys, 2004) impair mentalizing perform-ance. One exception is a study that Uta Frithwas involved with (Bird, Castelli, Malik, Frith,& Husain, 2004). The researchers studied apatient with damage to much of her frontalcortex, including the whole of mPFC.

Figure 3. Activity when subjects watch animations that involve

mental state attribution to triangles relative to animations that

show triangles moving randomly (from Castelli et al., 2000) in

the medial prefrontal cortex (mPFC; left panel) and superior

temporal sulcus/temporo-parietal junction (STS/TPJ; right panel).

Figure 1. Activity during reading stories that involve mental state

attribution relative to unlinked sentences (from Fletcher et al.,

1995), in (1) the temporal poles bilaterally, (2) the precuneus/posterior cingulate, (3) left superior temporal sulcus (STS), and

(4) medial prefrontal cortex (mPFC).

Figure 2. Activity when subjects think about intentions compared

with thinking about physical events (from den Ouden et al.,

2005) in (1) the medial prefrontal cortex (mPFC) and (2)

superior temporal sulcus/temporo-parietal junction (STS/TPJ).

42 THE QUARTERLY JOURNAL OF EXPERIMENTAL PSYCHOLOGY, 2008, 61 (1)

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Surprisingly (given the neuroimaging literature),the patient showed normal performance on men-talizing tasks. Whether this rules out mPFC asbeing necessary for mentalizing, or whether thispatient’s good performance was because of neur-onal reorganization, is unclear. Uta often saysthat surprising results, results that one wouldnever predict, can be more important than pre-dicted results. This is a clear example of a surpris-ing result, which needs to be considered in theoriesof mPFC function.

The roles of the different regions in mentaliz-ing are the subject of much debate. The mPFCis activated when subjects think about psychologi-cal states even if those states are applied to animals(Mitchell, Banaji, & Macrae, 2005). The mPFC isalso activated by tasks that involve thinking aboutmental states in relation to the self (Johnson et al.,2002; Lou et al., 2004; Ochsner et al., 2004;Vogeley et al., 2001). Games that involve surmis-ing an opponent’s mental states also activate themPFC (e.g., Gallagher, Jack, Roepstorff, &Frith, 2002; McCabe, Houser, Ryan, Smith, &Trouard, 2001). All of these tasks involve thinkingabout mental states. One prominent theory ofmPFC function is that it is activated wheneversubjects reflect on mental states (e.g., Amodio &Frith, 2006). Frith (C. D. Frith, 2007) has pro-posed that the mPFC is involved in the necessarydecoupling of mental states from reality. Activityin mPFC is often observed during rest conditionsin comparison with higher demand tasks (includ-ing mentalizing; Gusnard & Raichle, 2001). Ithas been suggested that, during rest or low-demand tasks, participants might indulge in spon-taneous mentalizing (Amodio & Frith, 2006).

The STS has been proposed to play a role in theprediction of observed patterns of behaviour inorder to surmise the mental states underlyingthis behaviour (C. D. Frith, 2007; C. D. Frith &Frith, 2006; U. Frith & Frith, 2003). Thisregion is activated during the perception of bio-logical motion (e.g., Allison, Puce, & McCarthy,2000; Grezes et al., 2001; Grossman et al.,2000), faces and body parts (e.g., Campbellet al., 2001; Chao, Haxby, & Martin, 1999;Puce, Allison, Bentin, Gore, & McCarthy, 1998)

and eye movements (e.g., Pelphrey, Morris,Michelich, Allison, & McCarthy, 2005). Onepossibility is that this region is involved in predict-ing observed movements (C. D. Frith, 2007).

In summary, a network of brain regions includ-ing mPFC and STS/TPJ seems to be involved inmany aspects of social cognition. In the nextsection I review evidence that these brain regionsdevelop over several decades in humans.

Development of social cognition

There is a rich literature on the development ofsocial cognition in infancy and childhood, andhere I will not go into any detail (this literatureis reviewed in papers by Perner & Leekham,2008; Sodian, 2008). Signs of social competencedevelop during early infancy, such that by around12 months of age infants can ascribe agency to asystem or entity (Johnson, 2003; Spelke, Phillips,&Woodward, 1995). The understanding of inten-tion emerges at around 18 months, when infantsacquire joint attention skills—for example, theyare able to follow an adult’s gaze towards a goal(Carpenter, Nagell, & Tomasello, 1998). Theseearly social abilities precede more explicit menta-lizing, such as false-belief understanding, whichusually emerges by about four or five years(Barresi & Moore, 1996). While normally devel-oping children begin to pass Theory of Mindtasks by age five, the brain structures that underliementalizing (mPFC and STS/TPJ) undergo sub-stantial development well beyond early childhood.These studies are reviewed in the next section.

Cellular development in the brain duringadolescence

The notion that the brain continues to developafter childhood is relatively new. Experiments onanimals, starting in the 1950s, showed thatsensory regions of the brain go through sensitiveperiods soon after birth, during which timeenvironmental stimulation appears to be crucialfor normal brain development and for normal per-ceptual development to occur (Hubel & Wiesel,1962). These experiments suggested that thehuman brain might be susceptible to the same



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sensitive periods in early development. Researchon postmortem human brains carried out in the1970s revealed that some brain areas, in particularthe PFC, continue to develop well beyond earlychildhood (Huttenlocher, 1979; Huttenlocher,De Courten, Garey, & Van Der Loos, 1983;Yakovlev & Lecours, 1967).

Two main changes were found in the brainbefore and after puberty. As neurons develop, alayer of myelin is formed around their axon.Myelin acts as an insulator and significantlyincreases the speed of transmission of electricalimpulses from neuron to neuron. While sensoryand motor brain regions become fully myelinatedin the first few years of life, axons in the frontalcortex continue to be myelinated well into adoles-cence (Yakovlev & Lecours, 1967). The implicationof this research is that the transmission speed ofneural information in the frontal cortex mightincrease throughout childhood and adolescence.

The second difference in the brains of prepu-bescent children and adolescents pertains tochanges in synaptic density in PFC. Early in post-natal development, the brain begins to form newsynapses, so that the synaptic density (thenumber of synapses per unit volume of braintissue) greatly exceeds adult levels. This processof synaptogenesis lasts up to several months,depending on the species of animal and the brainregion. These early peaks in synaptic density arefollowed by a period of synaptic elimination(pruning) in which frequently used connectionsare strengthened and infrequently used connec-tions are eliminated. This process, which occursover a period of years, reduces the overall synapticdensity to adult levels. In sensory regions of themonkey brain, synaptic densities graduallydecline to adult levels at around three years,around the time monkeys reach sexual maturity(Rakic, 1995).

In contrast to sensory brain regions, histologicalstudies of monkey and human PFC have shownthat there is a proliferation of synapses in the sub-granular layers of the PFC during childhood andagain at puberty, followed by a plateau phase anda subsequent elimination and reorganization ofprefrontal synaptic connections after puberty

(Bourgeois, Goldman-Rakic, & Rakic, 1994;Huttenlocher, 1979; Woo, Pucak, Kye, Matus,& Lewis, 1997; Zecevic & Rakic, 2001).According to these data, synaptic pruning occursthroughout adolescence and results in a netdecrease in synaptic density in the PFC duringthis time.

MRI studies of adolescent braindevelopment

Until recently, the structure of the human braincould be studied only after death. The scarcity ofpostmortem brains in research meant that knowl-edge of human brain development was limited.Since the advent of magnetic resonance imaging(MRI), a number of brain-imaging studies haveprovided further evidence of the ongoing matu-ration of the frontal cortex and other regions,into adolescence and even into adulthood. A con-sistent finding from both cross-sectional andlongitudinal MRI studies is that there is a steadyincrease in white matter (WM) in certain brainregions, particularly PFC and parietal cortex,during childhood and adolescence (e.g., Gieddet al., 1999; Giedd et al., 1996; Paus et al.,1999b; Pfefferbaum et al., 1994; Reiss, Abrams,Singer, Ross, & Denckla, 1996; Sowell et al.,2003; Sowell et al., 1999). Most studies point toa linear increase in white matter with age(Barnea-Goraly et al., 2005; Giedd et al., 1999;Paus et al., 1999a, 1999b; Pfefferbaum et al.,1994; Reiss et al., 1996; Sowell et al., 1999). Inlight of histological studies, this has been inter-preted as reflecting continued axonal myelinationduring childhood and adolescence.

While the increase in white matter in certainbrain regions seems to be linear, changes in greymatter (GM) density appear to follow a region-specific, nonlinear pattern. Several studies haveshown that GM development in certain brainregions follows an inverted-U shape. In one ofthe first developmental MRI studies, Gieddet al., (1999) performed a longitudinal MRIstudy on 145 healthy boys and girls ranging inage from about 4 to 22 years. The volume ofGM in the frontal lobe increased during


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preadolescence with a peak occurring at around 12years for males and 11 years for females. This wasfollowed by a decline during postadolescence.Similarly, parietal lobe GM volume increasedduring the preadolescent stage to a peak ataround 12 years for males and 10 years forfemales, and this was followed by decline duringpostadolescence. GM development in the tem-poral lobes was also nonlinear, and the peak wasreached later at about 17 years. A similarinverted-U shaped developmental trajectory ofGM in various cortical regions has been found inseveral subsequent MRI studies (e.g., Gogtayet al., 2004; Thompson et al., 2000). Moststudies show that sensory and motor regionsmature first, while PFC and parietal and temporalcortices continue to develop during adolescenceand beyond.

In summary, several recent MRI studies havesuggested that a perturbation in GM densitymore or less coincides with the onset of pubertyin some cortical regions. This has been interpretedas reflecting the synaptic reorganization thatoccurs at the onset of puberty (Bourgeois et al.,1994; Huttenlocher, 1979). Thus, the increase inGM apparent at the onset of puberty (Gieddet al., 1999) might reflect a wave of synapse pro-liferation at this time, while the gradual decreasein GM density that occurs after puberty has beenattributed to postpubescent synaptic pruning.

The brain regions that undergo protracteddevelopment include PFC, parietal cortex andsuperior temporal cortex (in some studies thishas included STS). As discussed above, these areregions that are implicated in social cognition inadults. The effect of continued neural develop-ment in brain regions associated with social cogni-tion is largely unknown. Only a relatively smallnumber of studies have investigated social cogni-tive function during adolescence.

Development of social cognitionduring adolescence

While there is a wealth of social psychologyresearch on socio-emotional processing in adoles-cence, there is surprisingly little empirical research

on social cognitive development during thisperiod. One area of social processing that hasbeen studied in the context of adolescence is faceprocessing, perhaps because early behaviouralstudies of face processing found evidence for aninterruption at puberty in the developmentalcourse of face recognition (Carey, Diamond, &Woods, 1980; Diamond, Carey, & Back, 1983).In one study the percentage of correct responsesin a behavioural face recognition task improvedby over 20% between the ages of 6 and 10 anddeclined by about 10% around the age of puberty(Carey et al., 1980). Performance on the taskrecovered again during adolescence. In anotherstudy, face encoding was found to be worse in pub-escent girls than in pre- and postpubescent girlsmatched for age (Diamond et al., 1983).

Recently, several groups have investigated theneural processing of facial expressions of emotionin adolescents. Thomas et al. (2001) investigatedamygdala activation to fearful facial expressionsin a group of children (mean age 11 years) andadults. Adults demonstrated greater amygdalaactivation to fearful facial expressions, whereaschildren showed greater amygdala activation toneutral faces. Slightly different results wereobtained by Killgore, Oki, and Yurgelun-Todd(2001). Results indicated sex differences in amyg-dala development: Although the left amygdalaresponded to fearful facial expressions in all chil-dren, left amygdala activity decreased over theadolescent period in females but not in males.Females also demonstrated greater activation ofthe dorsolateral PFC over this period, whereasmales demonstrated the opposite pattern. In arecent study, bilateral PFC activity increasedwith age (from 8 to 15 years) for girls, whereasonly activity in right PEC was correlated withage in boys (Yurgelun-Todd & Killgore, 2006).

In a recent study, a group of adolescents (aged 7to 17) and a group of adults (aged 25–36) viewedfaces showing emotional expressions. Whileviewing faces with fearful emotional expressions,adolescents exhibited greater activation thanadults of the amygdala, orbitofrontal cortex, andanterior cingulate cortex (Monk et al., 2003).When subjects were asked to switch their attention



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between a salient emotional property of the face(thinking about how afraid it makes them feel)and a nonemotional property (how wide is thenose), adults, but not adolescents, selectivelyengaged and disengaged the orbitofrontal cortex.These functional MRI (fMRI) results suggestthat both emotion processing and cognitiveappraisal systems develop during adolescence.

A recent fMRI study investigated the develop-ment during adolescence of the neural networkunderlying thinking about intentions (Blakemore,den Ouden, Choudhury, & Frith, 2007). In thisstudy, 19 adolescent participants (aged 12.1 to18.1 years), and 11 adults (aged 22.4 to 37.8years), were scanned using fMRI. A factorialdesign was employed with between-subjectsfactor age group and within-subjects factor causality(intentional or physical). In both adults andadolescents, answering questions about intentionalcausality versus physical causality activated thementalizing network, including medial PFC,STS and temporal poles. In addition, there was asignificant interaction between group and task inthe medial PFC. During intentional relative tophysical causality, adolescents activated part ofthe medial PFC more than did adults and adultsactivated part of the right STS more than didadolescents. These results suggest that the neuralstrategy for thinking about intentions changesbetween adolescence and adulthood. Althoughthe same neural network is active, the relativeroles of the different areas change, with activitymoving from anterior (medial prefrontal) regionsto posterior (temporal) regions with age.

While face processing is an example of an areaof social cognitive development during adoles-cence that has received attention in recent years,very little is known about how other aspects ofsocial cognition change during the teenageyears. It appears paradoxical that the some ofthe brain regions involved in social cognitionundergo such dramatic development into adoles-cence, when the functions mediated by theseregions (e.g., ToM) appear to mature muchearlier. If an ability (such as passing a ToMtask) is accomplished by early to mid childhood,it is unlikely that it will undergo dramatic

changes beyond that time. One possibility isthat neural development during adolescenceinfluences more subtle abilities, such as thecapacity to modulate social cognitive processesin the context of everyday life. Another possibilityis that tasks that tap into implicit social cognitiveprocesses might be more likely to undergo changeduring adolescence. We have recently found someevidence for this in the domain of action imagery(Choudhury, Bird, Charman, & Blakemore,2007, in press). However, in the realm of devel-opment of social cognition during adolescence,there is a large gap in knowledge waiting to befilled.

CONCLUSION

After Uta Frith and colleagues’ seminal paper onthe neural processing of Theory of Mind(Fletcher et al., 1995), much has been learnedabout the social brain. There is a general consensusabout brain regions activated when subjects thinkabout mental states, though the exact role eachregion plays in Theory of Mind processing is stilldebated. Some of these brain regions undergo sub-stantial development during adolescence, which hasimplications for the development of social cogni-tion, in particular understanding other people.Social cognitive development during adolescenceis a new and rapidly expanding field. Many ques-tions remain unanswered. The role of hormones,culture and the social environment on the develop-ment of the social brain are unknown. It is possiblethat changes in hormones and social environment(for example, changing school) interact withneural development at the onset of puberty.Future research is needed to disentangle the contri-butions of biological and environmental factors tothe developing social brain.

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development of the social brain during adolescence

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